# Mechanism Study on the Regulation of Intestinal Microecology by Hangover Liver‐Protecting Beverage for the Treatment of Alcoholic Liver Disease

**Authors:** Wen Cai, Ping Wang, Ru Zhang, Limin Dong, Jiayi Li, Mingming Wang, Lin Wang, Xuekun Shao, Tianyuan Jing, Yanan Hu, Yi Wang, Cheng Wang, Tiefeng Sun, Haitao Du, Xiaoyan Ding

PMC · DOI: 10.1002/fsn3.71435 · 2026-01-07

## TL;DR

This study explores how a liver-protecting beverage made from natural ingredients helps treat alcoholic liver disease by improving gut health and reducing inflammation.

## Contribution

The study identifies active components in a food-based beverage and reveals its multi-target mechanisms in treating ALD through gut-liver interactions.

## Key findings

- HLB reduces liver injury markers like LPS, ALT, and AST in ALD model mice.
- HLB restores intestinal flora homeostasis and short-chain fatty acid metabolism.
- HLB inhibits the TLR4/NF-κB/NLRP3 inflammatory pathway in the liver.

## Abstract

In this study, we systematically investigated the preventive and curative effects of food‐sourced hangover liver‐protecting beverage (HLB) against alcoholic liver disease (ALD) and their multi‐target mechanisms through molecular docking, 16S rDNA sequencing, and functional assessment of the hepatic‐intestinal axis. Based on the theory of medicinal food harmony (MFH), 121 potential active components were identified from six foods, including 
Hovenia dulcis
, chicory, and umeboshi, by UPLC‐QTOF‐MS/MS technology. HLB characteristic active components such as quercetin, catechin, and ferulic acid were verified through molecular docking. In vivo experiments showed that HLB significantly reduced serum LPS, ALT, AST, TC, and TG levels, upregulated the expression of intestinal tight junction protein (ZO‐1/Occludin), and inhibited the activation of the TLR4 (Toll‐like receptor 4)/NF‐κB/NLRP3 inflammatory axis in ALD model mice. Meanwhile, HLB restored the homeostasis of intestinal flora and the metabolism of short‐chain fatty acids (SCFAs), confirming that it synergistically ameliorated liver injury through the “flora‐SCFAs‐intestinal barrier” axis. This study reveals the molecular basis for the regulation of ALD by food‐based natural ingredients through liver – gut interactions and provides theoretical and practical basis for the development of functional beverages with both safety and multi‐target effects.

Technical Roadmap for HLB‐Mediated ALD Therapy.

## Linked entities

- **Genes:** TLR4 (toll like receptor 4) [NCBI Gene 7099], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], TJP1 (tight junction protein 1) [NCBI Gene 7082], si:ch73-61d6.3 (uncharacterized si:ch73-61d6.3) [NCBI Gene 103182021]
- **Proteins:** TLR4 (toll like receptor 4), NFKB1 (nuclear factor kappa B subunit 1), NLRP3 (NLR family pyrin domain containing 3), TJP1 (tight junction protein 1), si:ch73-61d6.3 (uncharacterized si:ch73-61d6.3)
- **Chemicals:** quercetin (PubChem CID 5280343), catechin (PubChem CID 1203), ferulic acid (PubChem CID 445858), ALT (PubChem CID 10219674), TC (PubChem CID 23957), TG (PubChem CID 2723601)
- **Diseases:** alcoholic liver disease (MONDO:0043693), ALD (MONDO:0010247)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** ALD (MESH:D008108), inflammatory (MESH:D007249), liver injury (MESH:D017093)
- **Chemicals:** TG (MESH:D013866), Hangover Liver (-), quercetin (MESH:D011794), SCFAs (MESH:D005232), catechin (MESH:D002392), TC (MESH:D013667), LPS (MESH:D008070), ferulic acid (MESH:C004999)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12778415/full.md

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Source: https://tomesphere.com/paper/PMC12778415